Phagocyte-derived reactive oxygen species do not influence the progression of murine blood-stage malaria infections.

functional NADPH oxidase and thus the ability to produce phagocyte-derived reactive oxygen species. We found that the absence of functional NADPH oxidase in the gene knockout mice had no effect on the parasitemia or total parasite burden in mice infected with either resolving (Plasmodium yoelii and Plasmodium chabaudi K562) or fatal (Plasmodium berghei ANKA, Plasmodium berghei K173 and Plasmodium vinckei vinckei) strains of malaria. This lack of effect was apparent in both primary and secondary infections with P. yoelii and P. chabaudi. There was also no difference in the presentation of clinical or pathological signs between the gp91 phox/ or wild-type strains of mice infected with malaria. Progression of P. berghei ANKA and P. berghei K173 infections was unchanged in glutathione peroxidase-1 gene knockout mice compared to their wild-type counterparts. The rates of parasitemia progression in gp91 phox/ mice and wild-type mice were not significantly different when they were treated with L-N G -methylarginine, an inhibitor of nitric oxide synthase. These results suggest that phagocyte-derived reactive oxygen species are not crucial for the clearance of malaria parasites, at least in murine models. Malaria is an enormous health, social, and economic burden for over 40% of the world’s population. More than half a billion people are infected with malaria each year, and many of these infections result in chronic parasitemia and anemia. It is believed that phagocytic cells such as monocytes are important in the clearance of the blood-stage parasite (42, 53). However, the mechanism by which monocytes and other phagocytic cells effect killing of the parasite is as yet unknown.